These studies have been directed towards the analysis of the mode of operation of the mechanisms controlling information transmission from primary afferents to second order cells. In the unanesthetized spinal cord of the cat, stimulation of group I afferents in flexor nerves could reduce the mean peak amplitude and the peak variance of the monosynaptic Ia EPSPs evoked in gastrocnemius motoneurons often without affecting the mean peak amplitude and peak variance of the monosynaptic component of the EPSPs evoked by stimulation of the ipsilateral ventral funiculus (VF). In most cases the Ia and VF monosynaptic EPSPs elicited in the same motoneuron summated non-linearly, suggesting that both species of fibers ended in "electrotonically close" synaptic loci over the motoneuron surface. These observations suggest that the Ia EPSP mean and variance changes are mediated, at least in part, through a presynaptic mechanism, presumably through the segmental paths mediating the primary afferent depolarization (PAD), and that impulse transmission through VF terminals is not subjected to such a presynaptic control mechanism. An additional objective of our investigations has been to analyze the possible role of GABA in the generation of PAD in the frog spinal cord. For this, we correlated the intraspinal distribution of H3-GABA uptake with the distribution of the field potentials generated during the PAD produced by antidromic stimulation of motor nerves. The close parallelism in the spatial distribution of the two suggests that the elements that take up GABA are indeed located in the same general region where PAD is originated. This is considered as a necessary, although not sufficient, condition for the involvement of GABA in the generation of PAD.